Synthetic heptapeptide analog of the endogenous immunomodulator tuftsin, extended with a Pro-Gly-Pro tail for metabolic stability. Studied in GABA-receptor modulation, anxiety and stress models, enkephalin metabolism, and neuroimmune signaling. 99%+ purity confirmed by independent HPLC-MS; lot COA published before sale.
Independent laboratory testing confirms purity and composition of this research material.
Selank was developed at the Institute of Molecular Genetics, Russian Academy of Sciences, from tuftsin — the Thr-Lys-Pro-Arg tetrapeptide fragment of immunoglobulin G that stimulates phagocytosis. Adding Pro-Gly-Pro to the C-terminus stabilizes the peptide against degradation and, unexpectedly, produced a compound with pronounced anxiolytic activity in animal models alongside its immunomodulatory effects. It is the anxiety-related pharmacology, and its interaction with the GABAergic system, that has driven most subsequent research.
| Size | 10 mg lyophilized powder, 3 mL clear glass vial |
|---|---|
| Purity | ≥ 99% by HPLC; identity confirmed by LC-MS |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Molecular formula | C₃₃H₅₇N₁₁O₉ |
| Molecular weight | 751.9 Da |
| CAS | 129954-34-3 |
| Appearance | White lyophilized powder |
| Solubility | Water |
| Storage | −20 °C long term; 2–8 °C short term |
| Testing | Lot-specific COA from Janoshik Analytical |
Selank reduces anxiety-like behavior in elevated-plus-maze, open-field, and stress-paradigm studies in rodents without the sedation or motor impairment typical of benzodiazepines — the comparison most often drawn in the literature.
The peptide alters GABA-A receptor subunit expression and modulates the effect of GABA at its receptor, providing a non-benzodiazepine model of allosteric GABA-system regulation.
Selank inhibits enkephalin-degrading enzymes, raising endogenous enkephalin levels — a mechanism shared with Semax and relevant to pain and mood research.
Consistent with its tuftsin origin, Selank modulates interleukin-6, T-helper cytokine balance, and interferon expression, and is studied at the intersection of immune activation and behavior.
Secondary findings include improved retention in passive-avoidance tasks and modulation of BDNF expression in hippocampus.
Selank’s anxiolytic effect is attributed to GABA-A receptor modulation and increased enkephalin tone, with downstream effects on serotonin and norepinephrine turnover. It up-regulates BDNF expression and shifts gene expression in the hippocampus and frontal cortex toward patterns associated with reduced stress reactivity. Its immune effects run through cytokine regulation rather than direct receptor agonism.
Key papers include Kozlovskaya et al. (2003, Neuroscience and Behavioral Physiology) on anxiolytic activity, Volkova et al. (2016, Frontiers in Pharmacology) on GABA-A receptor gene expression, and Uchakina et al. (2008) on cytokine modulation. A comparative clinical study against a benzodiazepine is reported in Zozulya et al. (2008, Neuroscience and Behavioral Physiology). Selank is registered as a pharmaceutical in Russia; it has no regulatory status in the US.
Different parent peptides, different primary research areas. Selank derives from tuftsin and is studied mainly in anxiety, GABAergic, and immune models; Semax derives from ACTH(4–10) and is studied mainly in neurotrophin and neuroprotection models. See Semax.
No — this is the parent Thr-Lys-Pro-Arg-Pro-Gly-Pro sequence.
Match the lot number on your vial to the COA on the Lab Results page.
Every lot is analyzed by Janoshik Analytical, an independent accredited laboratory, before listing. Testing covers identity (LC-MS), purity (HPLC), net content, and endotoxin (LAL assay, USP <85>). The COA is published to the Lab Results page before the lot goes on sale.
Sealed lyophilized vials remain stable up to 24 months at −20 °C. Refrigerate at 2–8 °C on arrival and for short-term holding, protected from light and moisture. Avoid repeated freeze–thaw cycles.
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